Diabetes fuels periodontal lesions via GLUT1-driven macrophage inflammaging.

ABSTRACT: Hyperglycemia induces chronic low-grade inflammation (inflammaging), which is a newly identified contributor to diabetes-related tissue lesions, including the inflammatory bone loss in periodontitis. It is also a secondary senescent pattern mediated by an increased burden of senescent cells and senescence-associated secretory phenotype (SASP). Macrophage is a key SASP-spreading cell and may contribute to the maintenance of SASP response in the periodontal microenvironment. Using a transgenic diabetic model (BLKS/J-Lepr^db/lepr^db mice) we identified striking senescence of the periodontium in young (18-wk)-diabetic mice accompanied by amassed p16⁺-macrophages and enhanced early SASP response. Exposed to high glucose in vitro, bone marrow-derived macrophage (BM

SUBMITTER: Wang Q 

PROVIDER: S-EPMC7990943 | biostudies-literature | 2021 Mar

REPOSITORIES: biostudies-literature